【摘 要】
：
Hippocampal long-term potentiation(LTP)can be temporally and mechanistically classified into early phase LTP(E-LTP)and late phase LTP(L-LTP).While the non-decaying nature of L-LTP is thought to be dep
【机 构】
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Division of Neurology,Department of Medicine and Brain Research Centre,University of British Columbi
【出 处】
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第九届海内外华人神经科学家研讨会(The 9th Symposium for Chinese Neuroscientis
论文部分内容阅读
Hippocampal long-term potentiation(LTP)can be temporally and mechanistically classified into early phase LTP(E-LTP)and late phase LTP(L-LTP).While the non-decaying nature of L-LTP is thought to be dependent on protein synthesis and contributes to memory maintenance,little is known about the mechanisms and roles of the decaying E-LTP.Here,we demonstrate that inhibiting endocytosis of postsynaptic α-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid receptors(AMPARs)prevents the decay of E-LTP,thereby converting it into L-LTP.Conversely,releasing AMPAR endocytosis by inhibiting PKMζ causes L-LTP to decay,thereby converting it into E-LTP.Similarly,inhibition of AMPAR endocytosis is able to prolong memory retention in normal animals,and reduce memory loss in Alzheimers transgenic mice.These results strongly suggest that the decay of E-LTP is mediated by an active process involving AMPAR endocytosis,and inhibiting this process can prolong the longevity of LTP as well as memory under both physiological and pathological conditions.
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